The goal of this protocol is to determine whether staphylococcal toxins (super antigens) contribute to the T cell activation found in atopic dermatitis (AD) and study the role of S. aureus infection in the pathogenesis of this common skin disease. Specific aim one determines whether AD is associated with a selective expansion of T cells in their skin lesion. Specific aim two examines whether the selective stimulation of T cells in AD is clonotypic or diverse by cloning and sequencing the individual T cell receptor (TCR) transcripts amplified from AD skin lesions. The final specific aim investigates whether S. aureus growing on the skin of patients with an exacerbation of AD due to infection, produce toxins known to act as bacterial super antigens e.g. staphylococcal enterotoxins (SEs) and correlate these findings with the TCR V' gene usage of the T cell infiltrate from skin biopsies of the culture site. In addition, nonlesional skin of patients with AD and normal controls will be patch tested with staphylococcal exotoxins to determine if they can induce eczematoid skin lesions. Preliminary studies demonstrate that skin homing T cells in AD are associated with expansion of superantigen-reactive T cells. Patch testing induces eczematoid dermatitis associated with V-beta skewing consistent with a super antigen effect.